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http://purl.uniprot.org/citations/24008408http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/24008408http://www.w3.org/2000/01/rdf-schema#comment"

Purpose

The objective of this study was to elucidate the signaling pathway through which cationic antimicrobial protein of 37 kDa (CAP37) mediates human corneal epithelial cell (HCEC) chemotaxis.

Methods

Immortalized HCECs were treated with pertussis toxin (10 and 1000 ng/mL), protein kinase C (PKC) inhibitors (calphostin c, 50 nM and Ro-31-8220, 100 nM), phorbol esters (phorbol 12,13-dibutyrate, 200 nM and phorbol 12-myristate 13-acetate, 1 μM) known to deplete PKC isoforms, and siRNAs (400 nM) before a modified Boyden chamber assay was used to determine the effect of these inhibitors and siRNAs on CAP37-directed HCEC migration. PKCδ protein levels, PKCδ-Thr(505) phosphorylation, and PKCδ kinase activity was assessed in CAP37-treated HCECs using immunohistochemistry, Western blotting, and a kinase activity assay, respectively.

Results

Chemotaxis studies revealed that treatment with pertussis toxin, PKC inhibitors, phorbol esters, and siRNAs significantly inhibited CAP37-mediated chemotaxis compared with untreated controls. CAP37 treatment increased PKCδ protein levels and led to PKCδ phosphorylation on residue Thr(505). Direct activation of PKCδ by CAP37 was demonstrated using a kinase activity assay.

Conclusions

These findings lead us to conclude that CAP37 is an important regulator of corneal epithelial cell migration and mediates its effects through PKCδ."xsd:string
http://purl.uniprot.org/citations/24008408http://purl.org/dc/terms/identifier"doi:10.1167/iovs.13-12054"xsd:string
http://purl.uniprot.org/citations/24008408http://purl.uniprot.org/core/author"Pereira H.A."xsd:string
http://purl.uniprot.org/citations/24008408http://purl.uniprot.org/core/author"Russell R.A."xsd:string
http://purl.uniprot.org/citations/24008408http://purl.uniprot.org/core/author"Logan S."xsd:string
http://purl.uniprot.org/citations/24008408http://purl.uniprot.org/core/author"Gonzalez M.L."xsd:string
http://purl.uniprot.org/citations/24008408http://purl.uniprot.org/core/author"Kasus-Jacobi A."xsd:string
http://purl.uniprot.org/citations/24008408http://purl.uniprot.org/core/author"Thavathiru E."xsd:string
http://purl.uniprot.org/citations/24008408http://purl.uniprot.org/core/author"Griffith G.L."xsd:string
http://purl.uniprot.org/citations/24008408http://purl.uniprot.org/core/date"2013"xsd:gYear
http://purl.uniprot.org/citations/24008408http://purl.uniprot.org/core/name"Invest Ophthalmol Vis Sci"xsd:string
http://purl.uniprot.org/citations/24008408http://purl.uniprot.org/core/pages"6712-6723"xsd:string
http://purl.uniprot.org/citations/24008408http://purl.uniprot.org/core/title"CAP37 activation of PKC promotes human corneal epithelial cell chemotaxis."xsd:string
http://purl.uniprot.org/citations/24008408http://purl.uniprot.org/core/volume"54"xsd:string
http://purl.uniprot.org/citations/24008408http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/24008408
http://purl.uniprot.org/citations/24008408http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/24008408
http://purl.uniprot.org/uniprot/P20160#attribution-2AED8A7BBEC3E099E07401BB56BA2716http://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/24008408
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http://purl.uniprot.org/uniprot/Q99075#attribution-2AED8A7BBEC3E099E07401BB56BA2716http://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/24008408
http://purl.uniprot.org/uniprot/Q05655#attribution-2AED8A7BBEC3E099E07401BB56BA2716http://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/24008408
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